copd (chronic obstructive pulmonary disease) dr. meg-angela christi amores
TRANSCRIPT
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COPD(Chronic Obstructive Pulmonary Disease)
Dr. Meg-angela Christi Amores
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COPD
• Global Initiative for Chronic Obstructive Lung Disease (GOLD)
• a disease state characterized by airflow limitation that is not fully reversible – Includes:• emphysema, chronic bronchitis, and small airways
disease
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COPD
• Emphysema – an anatomically defined condition characterized
by destruction and enlargement of the lung alveoli• Chronic Bronchitis– a clinically defined condition with chronic cough
and phlegm• Small airways disease– a condition in which small bronchioles are
narrowed
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Risk Factors
• Cigarette Smoking– Intensity: pack years (sticks/day for years)– most highly significant predictor of FEV1
• Airway responsiveness– asthma, chronic bronchitis, and emphysema are
variations of the same basic disease• Respiratory infections– Remains to be proven
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Risk Factors
• Occupational Exposures– general exposure to dust at work– coal mining, gold mining, and cotton textile dust
• Ambient Air pollution– living in urban compared to rural areas– Remains to be proven
• Passive, or Second-Hand, Smoking Exposure• Genetic Considerations
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Natural History
• Effect of cigarette smoking depends on intensity, timing during growth, basal function
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Pathophysiology
• Airflow obstruction– Determined by spirometry: FEV1 and FVC– chronically reduced ratio of FEV1/FVC– seldom shows large responses to inhaled
bronchodilators• Hyperinflation– "air trapping“– helps to compensate for airway obstruction
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Pathophysiology
• Gas Exchange– Nonuniform ventilation and ventilation-perfusion
mismatching
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Pathology
• Large Airway– Cigarette smoking often results in mucous gland
enlargement and goblet cell hyperplasia– proportional to cough and mucus production
• Small Airways• major site of increased resistance in most individuals
with COPD is in airways 2 mm diameter• goblet cell metaplasia and replacement of surfactant-
secreting Clara cells with mucus-secreting and infiltrating mononuclear inflammatory cells
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Pathology
• Lung Parenchyma– destruction of gas-exchanging airspaces– walls become perforated and later obliterated with
coalescence of small distinct airspaces into abnormal and much larger airspaces
– Macrophages accumulate – Centriacinar emphysema- most frequently
associated with cigarette smoking– Panacinar emphysema - usually observed in patients
with alpha1AT deficiency
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Clinical presentation
• History• cough, sputum production, and exertional dyspnea• exertional dyspnea, often described as increased effort
to breathe, heaviness, air hunger, or gasping, can be insidious• patient's ability to perform them has changed
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Clinical presentation
• Physical Findings– entirely normal physical examination – early – signs of active smoking, including an odor of
smoke or nicotine staining of fingernails– prolonged expiratory phase and expiratory
wheezing- more severe– signs of hyperinflation include a barrel chest and
enlarged lung volumes
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Laboratory Findings
• hallmark of COPD is airflow obstruction• Pulmonary function testing shows airflow
obstruction with a reduction in FEV1 and FEV1/FVC
• lung volumes may increase
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Treatment
• SMOKING cessation• Bronchodilators• Anticholinergic agents• Beta agonists• Inhaled Glucocorticoids• Oral Glucocorticoids• Theophylline• Oxygen
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Treatment
• General Medical Care• Pulmonary Rehabilitation• Lung Volume Reduction Surgery• Lung Transplantation